Patients with type 2 diabetes mellitus exhibit non-enzymatic glycation of lipoproteins that are considered proatherogenic modification contributing to increased susceptibility of patients with diabetes to atherosclerosis. We postulated that glycated lipoproteins might be associated with vascular outcome. To explore this, we studied the relationship between glycated HDL (gHDL) and glycated LDL (gLDL) with vascular function in African American diabetic patients. Total of 146 diabetic were enrolled over a 6 month period. Levels of plasma gHDL and gLDL were measured by enzyme-linked immunosorbent assay (ELISA). Microvascular function was assessed by vascular reactivity index (VRI). Large artery stiffness was assessed by carotid-femoral pulse wave velocity (PWV). Carotid intima-media thickness (C-IMT) was assessed by B-mode ultrasound image analysis. Mean patient age was 60±8 years, 64% were female. 80% had hypertension, 90% had dyslipidemia and 15% had chronic kidney disease. Mean HbA1c levels were 8.1±2.2%. Pearson correlation analysis showed no significant correlation between gHDL and gLDL. Multi-regression analysis revealed that gHDL was negatively associated with VRI (β= -0.006, p= 0.012; r2 = 0.276 for model) in the entire population and in the group of patients with good glycemic control (HbA1c ≤ 7.0; β= -0.007, p= 0.031; r2 = 0.312 for model); whereas gLDL was positively associated with CIMT (β= 0.045, p= 0.051; r2= 0.568 for model) after adjustment for other independent variables such as age, gender, stroke, smoking, hypertension, dyslipidemia, HbA1c, diabetes duration, HDLc, and LDLc.

In this cohort, data showed that gHDL was associated with microvascular function, whereas gLDL was mainly correlated with carotid intima media thickness. Further large study is needed to clarify mediating factors of these relationships.


A. Eluwole: None. A.M. Adedayo: None. F. Tedla: None. A. Kremer: None. N. Mastrogiovanni: None. C. Rosenberg: None. P. Dreizen: None. J. LaRosa: None. L. Salciccioli: None. M. Boutjdir: None. M. Banerji: Speaker's Bureau; Self; Merck & Co., Inc.. C. Brown: None. M. Salifu: None. J. Lazar: None. A. Bakillah: None.

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